Evidence map›Paper›PMID 24780320›Full record

ArticleLife sciences2014

Curcumin-primed exosomes mitigate endothelial cell dysfunction during hyperhomocysteinemia.

A Kalani, P K Kamat, P Chaturvedi, S C Tyagi, N Tyagi

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Life sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Strategies for Engineering of Extracellular Vesicles.International journal of molecular sciences · 2023
    Review
  13. Review
  14. Review
  15. Article
  16. Extracellular vesicles in vascular remodeling.Acta pharmacologica Sinica · 2022
    Review
  17. Review
  18. Review
  19. Review
  20. Review

6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

A KalaniDepartment of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY 40202, USA.
P K KamatDepartment of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY 40202, USA.
P ChaturvediDepartment of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY 40202, USA.
S C TyagiDepartment of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY 40202, USA.
N TyagiDepartment of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, KY 40202, USA. Electronic address: n0tyag01@louisville.edu.
University of Louisville · US

Funding

Mechanisms of Mitochondrial Dysfunction in Brain VasculatureR01HL107640 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, NEETU · 2012 to 2016
$1.8M
NHLBI NIH HHS HL107640NHLBI NIH HHS R01 HL107640
6 · The paper itself

Abstract

aimExosomes, the nano-units (<200 nm), released from diverse cell types in the extracellular body fluid, possess non-immunogenic property and ability to cross the blood-brain barrier (BBB). Since exosomes carry biological information from their cells of origin, we hypothesize that priming cells with potential therapeutic agents release improved cellular contents through exosomes. Curcumin possesses anti-oxidative and anti-inflammatory properties and provides a promising treatment for cerebral diseases and therefore, the aim of the study is to establish that mouse brain endothelial cells (MBECs) when primed with curcumin (7.5 μM), release an alleviated exosome population that can help recover the endothelial cell (EC) layer permeability. MAIN

methodsHomocysteine is a well-known causative factor of BBB disruption; therefore, homocysteine-treated ECs were used as a model of BBB disruption and curcumin-primed exosomes were utilized to check their potential for mitigating EC disruption. MBECs were treated with curcumin and exosomes were isolated by using ultracentrifugation and immunoprecipitation. Expression levels of junction proteins were detected by Western blot and immunocytochemistry assays. Endothelial cell permeability was analyzed with Fluorescein isothiocyanate-Bovine serum albumin (FITC-BSA) leakage assay using transwell permeable supports. KEY

findingsExosomes derived from curcumin-treated (primed) cells (CUR-EXO) alleviated oxidative stress, tight junctions (ZO-1, claudin-5, occludin), adherent junction (VE-cadherin) proteins and EC layer permeability induced during EC damage due to high homocysteine levels (hyperhomocysteinemia). SIGNIFICANCE: In conclusion, the study potentiates the use of CUR-EXO for cerebral diseases where drug delivery is still a challenge. The results also pave the way to novel translational therapies for cerebral diseases by maintaining and establishing therapeutic conservatories via primed exosomes.

Indexed as

AnimalsAntigens, CDAnti-Inflammatory Agents, Non-SteroidalBlotting, WesternBrainCadherin 5CadherinsCattleCell Membrane PermeabilityCells, CulturedClaudin-5CurcuminEndothelium, VascularExosomesFlow CytometryHyperhomocysteinemiaAntigens, CDAnti-Inflammatory Agents, Non-SteroidalCadherin 5CadherinsClaudin-5CurcuminOccludinSerum Albumin, BovineZonula Occludens-1 ProteinBlood–brain barrierCurcuminEndothelial cellsExosomesHomocysteineOxidative stressPermeabilityTight junctions

Identifiers

PMID24780320
PMCPMC4075120
OpenAlexW2019456646

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.